Prostagladins have been found to be effective agents in altering the basal and hormonal stimulated activity of various exocrine organs, including the stomach and pancreas. Previous research indicated that the prostaglandins A1 and E1 (PGAl and PGE1), produced significant changes in basal and hormonally stimulated bile flow. Present evidence suggests that cyclic AMP is an intracellular mediator of the response produced by the prostaglandins in other cell systems. It is possible, therefore, that alterations in basal and hormonally stimulated bile flow produced by the prostaglandins are mediated by cyclic AMP; and it is this concept that the present research is intended to evaluate. PGAl has been found to produce a bicarbonate rich choleresis suggesting that its effect is the result of changes produced in the ductal component of hepatic bile flow. PGA1 also decreases bile flow stimulated exogenous secretin administration again suggesting it acts at the ductal level. Recent evaluation of the effects of prostaglandin F2-alpha (PGF2-alpha) on bile flow has resulted in different findings. PGF2-alpha is a potent cholerectic agent producing increases in bile salt and chloride secretion. The increase in bile salt secretion, in the absence of changes in bicarbonate secretion, suggests that PGF2-alpha alters the bile salt dependent canalicular fraction of hepatic bile flow. Evaluation of cyclic AMP levels in bile during prostaglandin administration indicates that the increased bile salt secretion produced by PGF2-alpha is associated with decreased cyclic AMP levels in bile. Pursual of these avenues of research may lead to information which better delineates the intracellular mechanisms controlling bile salt secretion in hepatic bile. Such knowledge may afford to physicians methods to control and alter bile salt secretion.